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We measured the size of the spleen in 50 patients with RA (nine men, 41 women; average age 55.8 years (range 25–78)) and 14 healthy control subjects (no men, 14 women; average age 47.8 years (range 25–80)) by abdominal ultrasonography (Aloka, Japan). This examination was done by one skilful examiner (TD) in all cases, and comparisons were made with clinical profile and disease activity. The patients with a diagnosis of Felty's syndrome, categorised as the triad, RA, leucopenia, and splenomegaly, and patients with complications of any viral or bacterial infections were excluded from this study. Mean (SD) disease duration was 6.2 (6.6) years. The disease stage was I (13 patients), II (11), III (nine), IV (17) and the functional class was I (seven patients), II (40), III (three), IV (0), assigned according to Steinbrocker criteria.3 The following treatment was being used when the sonographic examination was performed: non-steroidal anti-inflammatory drugs (50 patients); gold treatment (12); sulfhydryl compounds (d-penicillamine or bucillamine, 26); sulfasalazine (24); methotrexate (16); cyclophosphamide (one); prednisolone (34: 31 patients <5 mg/d, two patients 7.5 mg/d, one patient 10 mg/d). A splenic index (SI) was calculated as the length of the longitudinal dimension × the transverse dimension in the coronal plane through the splenic hilum. These dimensions were obtained in each test with the subject in the supine position as described by Konuset al. 4 The cross sectional area of the spleen (CSAS) in the coronal plane through the splenic hilum was measured by calipers in 13 control subjects and 49 patients with RA. By application of an ultrasonic duplex system, splenic venous blood flow (SVBF) in eight control subjects and 47 patients with RA was calculated from the cross sectional area and the mean blood flow velocity in the splenic vein, according to the method described by Moriyasu et al.5 The SI in 50 patients with RA (mean (SD) 35.4 (8.1)) was significantly greater than that in control subjects (25.4 (5.0), p<0.0001, unpaired Student's t test). The CSAS and SVBF in patients with RA (28.0 (6.1) cm2, n=49; 301.0 (150.2) ml/min, n=47) were also significantly higher (p<0.0001, p<0.01) than in control subjects (20.5 (2.9) cm2, n=13; 139.1 (43.4) ml/min, n=8). The SI in all cases was significantly correlated with the CSAS (R 2=0.806, p<0.0001, n=62) and with SVBF (R 2=0.297, p<0.0001, n=55). From these results, an enlarged spleen was defined as an SI more than 35.4 (mean + 2SD of control subjects), and was diagnosed in 26/50 (52%) patients with RA. The average age of the patients with RA (55.8 years) differed by about eight years from that of control subjects (47.8 years). However, it is still certain that patients with RA have a larger spleen than control subjects because spleen size decreased with age in healthy subjects aged 18–65 according to a report by Niederau et al.6
Patients with RA were divided into two groups, those with an enlarged spleen (+) and those without (−), and clinical variables between the two groups were compared (table 1). There was no difference in the spleen size between patients with early or longstanding RA. Values of erythrocyte sedimentation rate and C reactive protein, as indicators of joint inflammation, were the same in both groups. Rheumatoid factor titres obtained by an RA haemagglutination assay in patients with RA with an enlarged spleen tended to be higher than in those without an enlarged spleen (p<0.2). There was no difference between either group of patients with RA in red blood cell counts, haemoglobin concentrations, or platelet cell counts. A significant difference was, however, found in the white blood cell counts (p<0.05). The number of patients receiving steroid treatment did not differ significantly between the two groups (χ2 test; 17/26v 17/24).
Defective reticuloendothelial system function in patients with RA was shown by determining the clearance of autologous, heat damaged erythrocytes from the circulation.7 An inverse correlation between splenic function and the level of circulating immune complexes was seen.7 We found that the number of white blood cells in patients with RA with an enlarged spleen detected by ultrasonography was significantly lower than in those without an enlarged spleen. These results indicated that an enlarged spleen in patients with RA might be caused by a mechanism similar to that in Felty's syndrome,1 in which white blood cells are sequestered in the spleen to clear the circulating immune complexes—that is, increased removal of granulocytes rather than impaired production of granulocytes. Overall, imaging the spleen in patients with RA with ultrasound is a more sensitive way (52%) to assess the size of the spleen than palpation on physical examination (5–10%). Furthermore, it is possible that 52% of patients with RA with a large spleen might be in the early stage of Felty's syndrome.
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